In order to solve the problem of genetic disorders in the central nervous system, there is an urgent need to develop a new field of science which directly investigates the gene-symptom relationship. The proposed study is designed to view the entire pathway from gene to resulting symptom in detail, thereby providing an ideal model for research of neurogenetic diseases. The neural mechanism underlying the genetic disorder in the central motor system is studied in neurological mutants of Drosophila melanogaster. Four single-gene mutants expressing specific leg movement disorders are produced in Canton-S stock of Drosophila melanogaster. These four different genes have already been located on X chromosome. All four of these mutants express leg-shaking disorders with patterns specific to each gene under the influence of ether. The neural mechanism underlying the leg-shaking disorders has already been studied, which disclosed the phenotype disorder to be expressed autonomously in certain neurons in leg motor regions. The mechanism of the disorders will be studied by recording electrical activities from those neurons intra- and extracellularly. The activity pattern of each neuron is then analyzed by a digital analyzer for quantitative description. Based on this analysis, the possible functional model of activity center for the disorder at each leg motor region of those four mutants is constructed. The functional model is later confirmed morphologically by histological techniques. The specific pattern coded by a gene can be modulated by the recombination of another gene. With this dual-gene mutant, the pattern formation mechanism is studied further in detail. The eag gene has a particular action to release the disorder coded by other genes in the absence of ether. Information thus obtained will elucidate the physiological mechanism of the genetic disorder in the motor system and the release mechanism of the genetic code stored in the neuron. BIBLIOGRAPHIC REFERENCES: Ikeda, K., S. Ozawa, and S. Hagiwara: Synaptic transmission reversibly conditioned by a single-gene mutation in Drosophila melanogaster. Nature 259, 489-491, 1976. Ikeda, K.: Genetically patterned neural activity. in Simpler Networks and Behavior, J.C. Fentress, ed., Sinauer Assoc., 1976.